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Journal articles on the topic 'Motor Neuron differentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Nango, Hiroshi, Yasuhiro Kosuge, Masaki Sato, et al. "Highly Efficient Conversion of Motor Neuron-Like NSC-34 Cells into Functional Motor Neurons by Prostaglandin E2." Cells 9, no. 7 (2020): 1741. http://dx.doi.org/10.3390/cells9071741.

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Motor neuron diseases are a group of progressive neurological disorders that degenerate motor neurons. The neuroblastoma × spinal cord hybrid cell line NSC-34 is widely used as an experimental model in studies of motor neuron diseases. However, the differentiation efficiency of NSC-34 cells to neurons is not always sufficient. We have found that prostaglandin E2 (PGE2) induces morphological differentiation in NSC-34 cells. The present study investigated the functional properties of PGE2-differentiated NSC-34 cells. Retinoic acid (RA), a widely-used agent inducing cell differentiation, facilitated neuritogenesis, which peaked on day 7, whereas PGE2-induced neuritogenesis took only 2 days to reach the same level. Whole-cell patch-clamp recordings showed that the current threshold of PGE2-treated cell action potentials was lower than that of RA-treated cells. PGE2 and RA increased the protein expression levels of neuronal differentiation markers, microtubule-associated protein 2c and synaptophysin, and to the same extent, motor neuron-specific markers HB9 and Islet-1. On the other hand, protein levels of choline acetyltransferase and basal release of acetylcholine in PGE2-treated cells were higher than in RA-treated cells. These results suggest that PGE2 is a rapid and efficient differentiation-inducing factor for the preparation of functionally mature motor neurons from NSC-34 cells.

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2

Lin, Yu-Lung, Yi-Wei Lin, Jennifer Nhieu, Xiaoyin Zhang, and Li-Na Wei. "Sonic Hedgehog-Gli1 Signaling and Cellular Retinoic Acid Binding Protein 1 Gene Regulation in Motor Neuron Differentiation and Diseases." International Journal of Molecular Sciences 21, no. 11 (2020): 4125. http://dx.doi.org/10.3390/ijms21114125.

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Cellular retinoic acid-binding protein 1 (CRABP1) is highly expressed in motor neurons. Degenerated motor neuron-like MN1 cells are engineered by introducing SODG93A or AR-65Q to model degenerated amyotrophic lateral sclerosis (ALS) or spinal bulbar muscular atrophy neurons. Retinoic acid (RA)/sonic hedgehog (Shh)-induced embryonic stem cells differentiation into motor neurons are employed to study up-regulation of Crabp1 by Shh. In SODG93A or AR-65Q MN1 neurons, CRABP1 level is reduced, revealing a correlation of motor neuron degeneration with Crabp1 down-regulation. Up-regulation of Crabp1 by Shh is mediated by glioma-associated oncogene homolog 1 (Gli1) that binds the Gli target sequence in Crabp1′s neuron-specific regulatory region upstream of minimal promoter. Gli1 binding triggers chromatin juxtaposition with minimal promoter, activating transcription. Motor neuron differentiation and Crabp1 up-regulation are both inhibited by blunting Shh with Gli inhibitor GANT61. Expression data mining of ALS and spinal muscular atrophy (SMA) motor neurons shows reduced CRABP1, coincided with reduction in Shh-Gli1 signaling components. This study reports motor neuron degeneration correlated with down-regulation in Crabp1 and Shh-Gli signaling. Shh-Gli up-regulation of Crabp1 involves specific chromatin remodeling. The physiological and pathological implication of this regulatory pathway in motor neuron degeneration is supported by gene expression data of ALS and SMA patients.

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3

Bax, Monique, Jessie McKenna, Dzung Do-Ha, et al. "The Ubiquitin Proteasome System Is a Key Regulator of Pluripotent Stem Cell Survival and Motor Neuron Differentiation." Cells 8, no. 6 (2019): 581. http://dx.doi.org/10.3390/cells8060581.

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The ubiquitin proteasome system (UPS) plays an important role in regulating numerous cellular processes, and a dysfunctional UPS is thought to contribute to motor neuron disease. Consequently, we sought to map the changing ubiquitome in human iPSCs during their pluripotent stage and following differentiation to motor neurons. Ubiquitinomics analysis identified that spliceosomal and ribosomal proteins were more ubiquitylated in pluripotent stem cells, whilst proteins involved in fatty acid metabolism and the cytoskeleton were specifically ubiquitylated in the motor neurons. The UPS regulator, ubiquitin-like modifier activating enzyme 1 (UBA1), was increased 36-fold in the ubiquitome of motor neurons compared to pluripotent stem cells. Thus, we further investigated the functional consequences of inhibiting the UPS and UBA1 on motor neurons. The proteasome inhibitor MG132, or the UBA1-specific inhibitor PYR41, significantly decreased the viability of motor neurons. Consistent with a role of the UPS in maintaining the cytoskeleton and regulating motor neuron differentiation, UBA1 inhibition also reduced neurite length. Pluripotent stem cells were extremely sensitive to MG132, showing toxicity at nanomolar concentrations. The motor neurons were more resilient to MG132 than pluripotent stem cells but demonstrated higher sensitivity than fibroblasts. Together, this data highlights the important regulatory role of the UPS in pluripotent stem cell survival and motor neuron differentiation.

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4

Hallam, S., E. Singer, D. Waring, and Y. Jin. "The C. elegans NeuroD homolog cnd-1 functions in multiple aspects of motor neuron fate specification." Development 127, no. 19 (2000): 4239–52. http://dx.doi.org/10.1242/dev.127.19.4239.

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The basic helix-loop-helix transcription factor NeuroD (Neurod1) has been implicated in neuronal fate determination, differentiation and survival. Here we report the expression and functional analysis of cnd-1, a C. elegans NeuroD homolog. cnd-1 expression was first detected in neuroblasts of the AB lineage in 14 cell embryos and maintained in many neuronal descendants of the AB lineage during embryogenesis, diminishing in most terminally differentiated neurons prior to hatching. Specifically, cnd-1 reporter genes were expressed in the precursors of the embryonic ventral cord motor neurons and their progeny. A loss-of-function mutant, cnd-1(ju29), exhibited multiple defects in the ventral cord motor neurons. First, the number of motor neurons was reduced, possibly caused by the premature withdrawal of the precursors from mitotic cycles. Second, the strict correlation between the fate of a motor neuron with respect to its lineage and position in the ventral cord was disrupted, as manifested by the variable expression pattern of motor neuron fate specific markers. Third, motor neurons also exhibited defects in terminal differentiation characteristics including axonal morphology and synaptic connectivity. Finally, the expression patterns of three neuronal type-specific transcription factors, unc-3, unc-4 and unc-30, were altered. Our data suggest that cnd-1 may specify the identity of ventral cord motor neurons both by maintaining the mitotic competence of their precursors and by modulating the expression of neuronal type-specific determination factors. cnd-1 appears to have combined the functions of several vertebrate neurogenic bHLH proteins and may represent an ancestral form of this protein family.

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5

Martinez-Morales, J. R., J. A. Barbas, E. Marti, P. Bovolenta, D. Edgar, and A. Rodriguez-Tebar. "Vitronectin is expressed in the ventral region of the neural tube and promotes the differentiation of motor neurons." Development 124, no. 24 (1997): 5139–47. http://dx.doi.org/10.1242/dev.124.24.5139.

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The extracellular matrix protein vitronectin and its mRNA are present in the embryonic chick notochord, floor plate and in the ventral neural tube at the time position of motor neuron generation. When added to cultures of neural tube explants of developmental stage 9, vitronectin promotes the generation of motor neurons in the absence of either notochord or exogenously added Sonic hedgehog. Conversely, the neutralisation of endogenous vitronectin with antibodies inhibits over 90% motor neuron differentiation in co-cultured neural tube/notochord explants, neural tube explants cultured in the presence of Sonic hedgehog, and in committed (stage 13) neural tube explants. Furthermore, treatment of embryos with anti-vitronectin antibodies results in a substantial and specific reduction in the number of motor neurons generated in vivo. These results demonstrate that vitronectin stimulates the differentiation of motor neurons in vitro and in vivo. Since the treatment of stage 9 neural tube explants with Sonic hedgehog resulted in induction of vitronectin mRNA expression before the expression of floor plate markers, we conclude that vitronectin may act either as a downstream effector in the signalling cascade induced by Sonic hedgehog, or as a synergistic factor that increases Shh-induced motor neuron differentiation.

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6

Pattyn, A., M. Hirsch, C. Goridis, and J. F. Brunet. "Control of hindbrain motor neuron differentiation by the homeobox gene Phox2b." Development 127, no. 7 (2000): 1349–58. http://dx.doi.org/10.1242/dev.127.7.1349.

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Motor neurons are a widely studied model of vertebrate neurogenesis. They can be subdivided in somatic, branchial and visceral motor neurons. Recent studies on the dorsoventral patterning of the rhombencephalon have implicated the homeobox genes Pax6 and Nkx2.2 in the early divergence of the transcriptional programme of hindbrain somatic and visceral motor neuronal differentiation. We provide genetic evidence that the paired-like homeodomain protein Phox2b is required for the formation of all branchial and visceral, but not somatic, motor neurons in the hindbrain. In mice lacking Phox2b, both the generic and subtype-specific programs of motoneuronal differentiation are disrupted at an early stage. Most motor neuron precursors die inside the neuroepithelium while those that emigrate to the mantle layer fail to switch on early postmitotic markers and to downregulate neuroepithelial markers. Thus, the loss of function of Phox2b in hindbrain motor neurons exemplifies a novel control point in the generation of CNS neurons.

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7

Lee, S., R. Shen, H. H. Cho, et al. "STAT3 promotes motor neuron differentiation by collaborating with motor neuron-specific LIM complex." Proceedings of the National Academy of Sciences 110, no. 28 (2013): 11445–50. http://dx.doi.org/10.1073/pnas.1302676110.

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8

Jungbluth, S., G. Koentges, and A. Lumsden. "Coordination of early neural tube development by BDNF/trkB." Development 124, no. 10 (1997): 1877–85. http://dx.doi.org/10.1242/dev.124.10.1877.

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Neurotrophins signal through members of the trk family of tyrosine kinase receptors and are known to regulate several neuronal properties. Although initially characterized by their ability to prevent naturally occurring cell death of subsets of neurons during development, neurotrophins can also regulate the proliferation and differentiation of precursor cells. Here we report a novel involvement of neurotrophins in early development of the neural tube. We demonstrate that a functional trkB receptor is expressed by motor neuron progenitors in the ventral neural tube and that treatment of ventral neural tube explants with the trkB ligand Brain-Derived Neurotrophic Factor (BDNF) leads to a significant increase in the number of motor neurons. The only BDNF expression detectable at this stage is by a subset of ventrally projecting interneurons in the dorsal neural tube; ablating this region in vivo leads to a reduction of motor neuron numbers. This loss can be prevented by simultaneous treatment with BDNF. We propose that BDNF produced by dorsal interneurons stimulates proliferation and/or differentiation of motor neuron progenitors after anterograde axonal transport and release in proximity to the trkB-expressing motor neuron precursors, thereby coordinating development between dorsal and ventral regions of the neural tube.

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9

Cave, Clinton, and Shanthini Sockanathan. "Transcription Factor Hand-offs “Enhance” Motor Neuron Differentiation." Neuron 92, no. 6 (2016): 1149–51. http://dx.doi.org/10.1016/j.neuron.2016.12.009.

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10

Rao, M. "Transmembrane Protein GDE2 Induces Motor Neuron Differentiation in Vivo." Science 309, no. 5744 (2005): 2212–15. http://dx.doi.org/10.1126/science.1117156.

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11

Cave, Clinton, and Shanthini Sockanathan. "Transcription factor mechanisms guiding motor neuron differentiation and diversification." Current Opinion in Neurobiology 53 (December 2018): 1–7. http://dx.doi.org/10.1016/j.conb.2018.04.012.

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12

Shin, Soojung, Stephen Dalton, and Steven L. Stice. "Human Motor Neuron Differentiation from Human Embryonic Stem Cells." Stem Cells and Development 14, no. 3 (2005): 266–69. http://dx.doi.org/10.1089/scd.2005.14.266.

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13

Pons, S., and E. Marti. "Sonic hedgehog synergizes with the extracellular matrix protein vitronectin to induce spinal motor neuron differentiation." Development 127, no. 2 (2000): 333–42. http://dx.doi.org/10.1242/dev.127.2.333.

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Patterning of the vertebrate neural tube depends on intercellular signals emanating from sources such as the notochord and the floor plate. The secreted protein Sonic hedgehog and the extracellular matrix protein Vitronectin are both expressed in these signalling centres and have both been implicated in the generation of ventral neurons. The proteolytic processing of Sonic hedgehog is fundamental for its signalling properties. This processing generates two secreted peptides with all the inducing activity of Shh residing in the highly conserved 19 kDa amino-terminal peptide (N-Shh). Here we show that Vitronectin is also proteolitically processed in the embryonic chick notochord, floor plate and ventral neural tube and that this processing is spatiotemporally correlated with the generation of motor neurons. The processing of Vitronectin produces two fragments of 54 kDa and 45 kDa, as previously described for Vitronectin isolated from chick yolk. The 45 kDa fragment lacks the heparin-binding domain and the integrin-binding domain, RGD, present in the non-processed Vitronectin glycoprotein. Here we show that N-Shh binds to the three forms of Vitronectin (70, 54 and 45 kDa) isolated from embryonic tissue, although is preferentially associated with the 45 kDa form. Furthermore, in cultures of dissociated neuroepithelial cells, the combined addition of N-Shh and Vitronectin significantly increases the extent of motor neuron differentiation, as compared to the low or absent inducing capabilities of either N-Shh or Vitronectin alone. Thus, we conclude that the differentiation of motor neurons is enhanced by the synergistic action of N-Shh and Vitronectin, and that Vitronectin may be necessary for the proper presentation of the morphogen N-Shh to one of its target cells, the differentiating motor neurons.

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14

Jang, Soomi, Young-Hoon Kang, Imran Ullah, et al. "Cholinergic Nerve Differentiation of Mesenchymal Stem Cells Derived from Long-Term Cryopreserved Human Dental Pulp In Vitro and Analysis of Their Motor Nerve Regeneration Potential In Vivo." International Journal of Molecular Sciences 19, no. 8 (2018): 2434. http://dx.doi.org/10.3390/ijms19082434.

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The reduction of choline acetyltransferase, caused by the loss of cholinergic neurons, leads to the absence of acetylcholine (Ach), which is related to motor nerve degeneration. The aims of the present study were to evaluate the in vitro cholinergic nerve differentiation potential of mesenchymal stem cells from cryopreserved human dental pulp (hDPSCs-cryo) and to analyze the scale of in vivo motor nerve regeneration. The hDPSCs-cryo were isolated and cultured from cryopreserved dental pulp tissues, and thereafter differentiated into cholinergic neurons using tricyclodecane-9-yl-xanthogenate (D609). Differentiated cholinergic neurons (DF-chN) were transplanted into rats to address sciatic nerve defects, and the scale of in vivo motor nerve regeneration was analyzed. During in vitro differentiation, the cells showed neuron-like morphological changes including axonal fibers and neuron body development, and revealed high expression of cholinergic neuron-specific markers at both the messenger RNA (mRNA) and protein levels. Importantly, DF-chN showed significant Ach secretion ability. At eight weeks after DF-chN transplantation in rats with sciatic nerve defects, notably increased behavioral activities were detected with an open-field test, with enhanced low-affinity nerve growth factor receptor (p75NGFR) expression detected using immunohistochemistry. These results demonstrate that stem cells from cryopreserved dental pulp can successfully differentiate into cholinergic neurons in vitro and enhance motor nerve regeneration when transplanted in vivo. Additionally, this study suggests that long-term preservation of dental pulp tissue is worthwhile for use as an autologous cell resource in the field of nerve regeneration, including cholinergic nerves.

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15

Chen, Weiqiang, Shuo Han, Weiyi Qian, et al. "Nanotopography regulates motor neuron differentiation of human pluripotent stem cells." Nanoscale 10, no. 7 (2018): 3556–65. http://dx.doi.org/10.1039/c7nr05430k.

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16

Tretiakova, Albina, and Lidiya Chebotariova. "Informativeness of neurophysiological diagnostic methods in the differentiation of motor neurons of spinal cord motor neuron disease." Ukrainian Neurosurgical Journal, no. 4 (December 5, 2013): 33–38. http://dx.doi.org/10.25305/unj.55412.

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17

Fullam, Timothy, and Jeffrey Statland. "Upper Motor Neuron Disorders: Primary Lateral Sclerosis, Upper Motor Neuron Dominant Amyotrophic Lateral Sclerosis, and Hereditary Spastic Paraplegia." Brain Sciences 11, no. 5 (2021): 611. http://dx.doi.org/10.3390/brainsci11050611.

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Following the exclusion of potentially reversible causes, the differential for those patients presenting with a predominant upper motor neuron syndrome includes primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), or upper motor neuron dominant ALS (UMNdALS). Differentiation of these disorders in the early phases of disease remains challenging. While no single clinical or diagnostic tests is specific, there are several developing biomarkers and neuroimaging technologies which may help distinguish PLS from HSP and UMNdALS. Recent consensus diagnostic criteria and use of evolving technologies will allow more precise delineation of PLS from other upper motor neuron disorders and aid in the targeting of potentially disease-modifying therapeutics.

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18

Hardwick, Laura J. A., and Anna Philpott. "xNgn2 induces expression of predominantly sensory neuron markers in Xenopus whole embryo ectoderm but induces mixed subtype expression in isolated ectoderm explants." Wellcome Open Research 3 (November 8, 2018): 144. http://dx.doi.org/10.12688/wellcomeopenres.14911.1.

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Proneural basic-helix-loop-helix (bHLH) proteins, such as Neurogenin2 (Ngn2) and Ascl1, are critical regulators at the onset of neuronal differentiation. Endogenously they have largely complementary expression patterns, and have conserved roles in the specification of distinct neuronal subtypes. In Xenopus embryos, xNgn2 is the master regulator of primary neurogenesis forming sensory, inter- and motor neurons within the neural plate, while xAscl1 is the master regulator of autonomic neurogenesis, forming noradrenergic neurons in the antero-ventral region of the embryo. Here we characterise neuronal subtype identity of neurons induced by xNgn2 in the ectoderm of whole Xenopus embryos in comparison with xAscl1, and in ectodermal “animal cap” explants. We find that the transcriptional cascades mediating primary and autonomic neuron formation are distinct, and while xNgn2 and xAscl1 can upregulate genes associated with a non-endogenous cascade, this expression is spatially restricted within the embryo. xNgn2 is more potent than xAscl1 at inducing primary neurogenesis as assayed by neural-β-tubulin. In ectoderm of the intact embryo, these induced primary neurons have sensory characteristics with no upregulation of motor neuron markers. In contrast, xNgn2 is able to up-regulate both sensory and motor neuron markers in naïve ectoderm of animal cap explants, suggesting a non-permissive environment for motor identity in the patterned ectoderm of the whole embryo.

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19

Perez, Lillian M., and Aixa Alfonso. "The Conserved ASCL1/MASH-1 Ortholog HLH-3 Specifies Sex-Specific Ventral Cord Motor Neuron Fate in Caenorhabditis elegans." G3: Genes|Genomes|Genetics 10, no. 11 (2020): 4201–13. http://dx.doi.org/10.1534/g3.120.401458.

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Neural specification is regulated by one or many transcription factors that control expression of effector genes that mediate function and determine neuronal type. Here we identify a novel role for one conserved proneural factor, the bHLH protein HLH-3, implicated in the specification of sex-specific ventral cord motor neurons in C. elegans. Proneural genes act in early stages of neurogenesis in early progenitors, but here, we demonstrate a later role for hlh-3. First, we document that differentiation of the ventral cord type C motor neuron class (VC) within their neuron class, is dynamic in time and space. Expression of VC class-specific and subclass-specific identity genes is distinct through development and is dependent on the VC position along the A-P axis and their proximity to the vulva. Our characterization of the expression of VC class and VC subclass-specific differentiation markers in the absence of hlh-3 function reveals that VC fate specification, differentiation, and morphology requires hlh-3 function. Finally, we conclude that hlh-3 cell-autonomously specifies VC cell fate.

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20

Mie, Masayasu, Mami Kaneko, Fumiaki Henmi, and Eiry Kobatake. "Induction of motor neuron differentiation by transduction of Olig2 protein." Biochemical and Biophysical Research Communications 427, no. 3 (2012): 531–36. http://dx.doi.org/10.1016/j.bbrc.2012.09.090.

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21

Tang, Yadong, Li Liu, Junjun Li, et al. "Effective motor neuron differentiation of hiPSCs on a patch made of crosslinked monolayer gelatin nanofibers." Journal of Materials Chemistry B 4, no. 19 (2016): 3305–12. http://dx.doi.org/10.1039/c6tb00351f.

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A patch made of crosslinked monolayer nanofibers was used for motor neuron differentiation from human induced pluripotent stem cells and plug-and-play with a commercial multi-electrode array for neuron spike recording.

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22

Pfaff, Samuel L., Monica Mendelsohn, Colin L. Stewart, Thomas Edlund, and Thomas M. Jessell. "Requirement for LIM Homeobox Gene Isl1 in Motor Neuron Generation Reveals a Motor Neuron– Dependent Step in Interneuron Differentiation." Cell 84, no. 2 (1996): 309–20. http://dx.doi.org/10.1016/s0092-8674(00)80985-x.

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23

Wang, Ning. "Stem Cells Go Soft: Pliant Substrate Surfaces Enhance Motor Neuron Differentiation." Cell Stem Cell 14, no. 6 (2014): 701–3. http://dx.doi.org/10.1016/j.stem.2014.05.007.

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24

Ben-Shushan, Etti, Eva Feldman, and Benjamin E. Reubinoff. "Notch Signaling Regulates Motor Neuron Differentiation of Human Embryonic Stem Cells." STEM CELLS 33, no. 2 (2015): 403–15. http://dx.doi.org/10.1002/stem.1873.

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25

Wang, Mengmeng, King-Hwa Ling, Jun Tan, and Cheng-Biao Lu. "Development and Differentiation of Midbrain Dopaminergic Neuron: From Bench to Bedside." Cells 9, no. 6 (2020): 1489. http://dx.doi.org/10.3390/cells9061489.

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Parkinson’s Disease (PD) is a neurodegenerative disorder affecting the motor system. It is primarily due to substantial loss of midbrain dopamine (mDA) neurons in the substantia nigra pars compacta and to decreased innervation to the striatum. Although existing drug therapy available can relieve the symptoms in early-stage PD patients, it cannot reverse the pathogenic progression of PD. Thus, regenerating functional mDA neurons in PD patients may be a cure to the disease. The proof-of-principle clinical trials showed that human fetal graft-derived mDA neurons could restore the release of dopamine neurotransmitters, could reinnervate the striatum, and could alleviate clinical symptoms in PD patients. The invention of human-induced pluripotent stem cells (hiPSCs), autologous source of neural progenitors with less ethical consideration, and risk of graft rejection can now be generated in vitro. This advancement also prompts extensive research to decipher important developmental signaling in differentiation, which is key to successful in vitro production of functional mDA neurons and the enabler of mass manufacturing of the cells required for clinical applications. In this review, we summarize the biology and signaling involved in the development of mDA neurons and the current progress and methodology in driving efficient mDA neuron differentiation from pluripotent stem cells.

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26

Sharp, David J., Wenqian Yu, Lotfi Ferhat, Ryoko Kuriyama, David C. Rueger, and Peter W. Baas. "Identification of a Microtubule-associated Motor Protein Essential for Dendritic Differentiation." Journal of Cell Biology 138, no. 4 (1997): 833–43. http://dx.doi.org/10.1083/jcb.138.4.833.

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The quintessential feature of the dendritic microtubule array is its nonuniform pattern of polarity orientation. During the development of the dendrite, a population of plus end–distal microtubules first appears, and these microtubules are subsequently joined by a population of oppositely oriented microtubules. Studies from our laboratory indicate that the latter microtubules are intercalated within the microtubule array by their specific transport from the cell body of the neuron during a critical stage in development (Sharp, D.J., W. Yu, and P.W. Baas. 1995. J. Cell Biol. 130:93– 104). In addition, we have established that the mitotic motor protein termed CHO1/MKLP1 has the appropriate properties to transport microtubules in this manner (Sharp, D.J., R. Kuriyama, and P.W. Baas. 1996. J. Neurosci. 16:4370–4375). In the present study we have sought to determine whether CHO1/MKLP1 continues to be expressed in terminally postmitotic neurons and whether it is required for the establishment of the dendritic microtubule array. In situ hybridization analyses reveal that CHO1/MKLP1 is expressed in postmitotic cultured rat sympathetic and hippocampal neurons. Immunofluorescence analyses indicate that the motor is absent from axons but is enriched in developing dendrites, where it appears as discrete patches associated with the microtubule array. Treatment of the neurons with antisense oligonucleotides to CHO1/MKLP1 suppresses dendritic differentiation, presumably by inhibiting the establishment of their nonuniform microtubule polarity pattern. We conclude that CHO1/MKLP1 transports microtubules from the cell body into the developing dendrite with their minus ends leading, thereby establishing the nonuniform microtubule polarity pattern of the dendrite.

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Sun, Xue-Jiao, Ming-Xing Li, Chen-Zi Gong, et al. "Temporal expression profiles of lncRNA and mRNA in human embryonic stem cell-derived motor neurons during differentiation." PeerJ 8 (November 13, 2020): e10075. http://dx.doi.org/10.7717/peerj.10075.

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Background Human embryonic stem cells (hESC) have been an invaluable research tool to study motor neuron development and disorders. However, transcriptional regulation of multiple temporal stages from ESCs to spinal motor neurons (MNs) has not yet been fully elucidated. Thus, the goals of this study were to profile the time-course expression patterns of lncRNAs during MN differentiation of ESCs and to clarify the potential mechanisms of the lncRNAs that are related to MN differentiation. Methods We utilized our previous protocol which can harvest motor neuron in more than 90% purity from hESCs. Then, differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) during MN differentiation were identified through RNA sequencing. Bioinformatic analyses were performed to assess potential biological functions of genes. We also performed qRT-PCR to validate the DElncRNAs and DEmRNAs. Results A total of 441 lncRNAs and 1,068 mRNAs at day 6, 443 and 1,175 at day 12, and 338 lncRNAs and 68 mRNAs at day 18 were differentially expressed compared with day 0. Bioinformatic analyses identified that several key regulatory genes including POU5F1, TDGF1, SOX17, LEFTY2 and ZSCAN10, which involved in the regulation of embryonic development. We also predicted 283 target genes of DElncRNAs, in which 6 mRNAs were differentially expressed. Significant fold changes in lncRNAs (NCAM1-AS) and mRNAs (HOXA3) were confirmed by qRT-PCR. Then, through predicted overlapped miRNA verification, we constructed a lncRNA NCAM1-AS-miRNA-HOXA3 network.

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Ruiz i Altaba, A. "Combinatorial Gli gene function in floor plate and neuronal inductions by Sonic hedgehog." Development 125, no. 12 (1998): 2203–12. http://dx.doi.org/10.1242/dev.125.12.2203.

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Within the developing vertebrate nervous system, it is not known how progenitor cells interpret the positional information provided by inducing signals or how the domains in which distinct groups of neural cells differentiate are defined. Gli proteins may be involved in these processes. In the frog neural plate, we have previously shown that the zinc finger transcription factor Gli1 is expressed in midline cells and mediates the effects of Shh inducing floor plate differentiation. In contrast, Gli2 and Gli3 are expressed throughout the neural plate except for the midline. Here, it is shown that Gli3 and Shh repress each other whereas Gli2, like Gli1, is a target of Shh signaling. However, only Gli1 can induce the differentiation of floor plate cells. In addition, Gli2 and Gli3 repress the ectopic induction of floor plate cells by Gli1 in co-injection assays and inhibit endogenous floor plate differentiation. The definition of the floor plate domain, therefore, appears to be defined by the antagonizing activities of Gli2 and Gli3 on Gli1 function. Because both Gli1 and Gli2 are induced by Shh, these results establish a regulatory feedback loop triggered by Shh that restricts floor plate cells to the midline. We have also previously shown that the Gli genes induce neuronal differentiation and here it is shown that there is specificity to the types of neurons the Gli proteins induce. Only Gli1 induces Nkx2.1/TTF-1(+) ventral forebrain neurons. Moreover, Gli2 and Gli3 inhibit their differentiation. In contrast, the differentiation of spinal motor neurons can be induced by the two ventrally expressed Gli genes, Gli1 and Gli2, suggesting that Gli2 directly mediates induction of motor neurons by Shh. In addition, Gli3 inhibits motor neuron differentiation by Gli2. Thus, combinatorial Gli function may pattern the neural tube, integrating positional information and cell type differentiation.

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Pfaender, Stefanie, Karl Föhr, Anne-Kathrin Lutz, et al. "Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem Cells." Neural Plasticity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/3760702.

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Disturbances in neuronal differentiation and function are an underlying factor of many brain disorders. Zinc homeostasis and signaling are important mediators for a normal brain development and function, given that zinc deficiency was shown to result in cognitive and emotional deficits in animal models that might be associated with neurodevelopmental disorders. One underlying mechanism of the observed detrimental effects of zinc deficiency on the brain might be impaired proliferation and differentiation of stem cells participating in neurogenesis. Thus, to examine the molecular mechanisms regulating zinc metabolism and signaling in differentiating neurons, using a protocol for motor neuron differentiation, we characterized the expression of zinc homeostasis genes during neurogenesis using human induced pluripotent stem cells (hiPSCs) and evaluated the influence of altered zinc levels on the expression of zinc homeostasis genes, cell survival, cell fate, and neuronal function. Our results show that zinc transporters are highly regulated genes during neuronal differentiation and that low zinc levels are associated with decreased cell survival, altered neuronal differentiation, and, in particular, synaptic function. We conclude that zinc deficiency in a critical time window during brain development might influence brain function by modulating neuronal differentiation.

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Turner, Martin R., Richard J. Barohn, Philippe Corcia, et al. "Primary lateral sclerosis: consensus diagnostic criteria." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 4 (2020): 373–77. http://dx.doi.org/10.1136/jnnp-2019-322541.

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Primary lateral sclerosis (PLS) is a neurodegenerative disorder of the adult motor system. Characterised by a slowly progressive upper motor neuron syndrome, the diagnosis is clinical, after exclusion of structural, neurodegenerative and metabolic mimics. Differentiation of PLS from upper motor neuron-predominant forms of amyotrophic lateral sclerosis remains a significant challenge in the early symptomatic phase of both disorders, with ongoing debate as to whether they form a clinical and histopathological continuum. Current diagnostic criteria for PLS may be a barrier to therapeutic development, requiring long delays between symptom onset and formal diagnosis. While new technologies sensitive to both upper and lower motor neuron involvement may ultimately resolve controversies in the diagnosis of PLS, we present updated consensus diagnostic criteria with the aim of reducing diagnostic delay, optimising therapeutic trial design and catalysing the development of disease-modifying therapy.

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Goodearl, A. D., A. G. Yee, A. W. Sandrock, G. Corfas, and G. D. Fischbach. "ARIA is concentrated in the synaptic basal lamina of the developing chick neuromuscular junction." Journal of Cell Biology 130, no. 6 (1995): 1423–34. http://dx.doi.org/10.1083/jcb.130.6.1423.

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ARIA is a member of a family of polypeptide growth and differentiation factors that also includes glial growth factor (GGF), neu differentiation factor, and heregulin. ARIA mRNA is expressed in all cholinergic neurons of the central nervous systems of rats and chicks, including spinal cord motor neurons. In vitro, ARIA elevates the rate of acetylcholine receptor incorporation into the plasma membrane of primary cultures of chick myotubes. To study whether ARIA may regulate the synthesis of junctional synaptic acetylcholine receptors in chick embryos, we have developed riboprobes and polyclonal antibody reagents that recognize isoforms of ARIA that include an amino-terminal immunoglobulin C2 domain and examined the expression and distribution of ARIA in motor neurons and at the neuromuscular junction. We detected significant ARIA mRNA expression in motor neurons as early as embryonic day 5, around the time that motor axons are making initial synaptic contacts with their target muscle cells. In older embryos and postnatal animals, we found ARIA protein concentrated in the synaptic cleft at neuromuscular junctions, consistent with transport down motor axons and release at nerve terminals. At high resolution using immunoelectron microscopy, we detected ARIA immunoreactivity exclusively in the synaptic basal lamina in a pattern consistent with binding to synapse specific components on the presynaptic side of the basal lamina. These results support a role for ARIA as a trophic factor released by motor neuron terminals that may regulate the formation of mature neuromuscular synapses.

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Jackson-Holmes, Emily L., Amanda W. Schaefer, Todd C. McDevitt, and Hang Lu. "Microfluidic perfusion modulates growth and motor neuron differentiation of stem cell aggregates." Analyst 145, no. 14 (2020): 4815–26. http://dx.doi.org/10.1039/d0an00491j.

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Patani, Rickie. "Generating Diverse Spinal Motor Neuron Subtypes from Human Pluripotent Stem Cells." Stem Cells International 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/1036974.

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Resolving the mechanisms underlying human neuronal diversification remains a major challenge in developmental and applied neurobiology. Motor neurons (MNs) represent a diverse pool of neuronal subtypes exhibiting differential vulnerability in different human neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). The ability to predictably manipulate MN subtype lineage restriction from human pluripotent stem cells (PSCs) will form the essential basis to establishing accurate, clinically relevantin vitrodisease models. I first overview motor neuron developmental biology to provide some context for reviewing recent studies interrogating pathways that influence the generation of MN diversity. I conclude that motor neurogenesis from PSCs provides a powerful reductionist model system to gain insight into the developmental logic of MN subtype diversification and serves more broadly as a leading exemplar of potential strategies to resolve the molecular basis of neuronal subclass differentiation within the nervous system. These studies will in turn permit greater mechanistic understanding of differential MN subtype vulnerability usingin vitrohuman disease models.

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Periz, Goran, Ye Yan, Zachary T. Bitzer та Shanthini Sockanathan. "GDP-bound Gαi2 regulates spinal motor neuron differentiation through interaction with GDE2". Developmental Biology 341, № 1 (2010): 213–21. http://dx.doi.org/10.1016/j.ydbio.2010.02.032.

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Tomassy, Giulio Srubek, Elvira De Leonibus, Denis Jabaudon, et al. "Area-specific temporal control of corticospinal motor neuron differentiation by COUP-TFI." Proceedings of the National Academy of Sciences 107, no. 8 (2010): 3576–81. http://dx.doi.org/10.1073/pnas.0911792107.

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Martinez, Alejandra M., Jovan Mirkovic, Zofia A. Stanisz, Fahmida S. Patwari, and Wan Seok Yang. "NSC ‐34 motor neuron‐like cells are sensitized to ferroptosis upon differentiation." FEBS Open Bio 9, no. 4 (2019): 582–93. http://dx.doi.org/10.1002/2211-5463.12577.

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Natarajan, Rajalaxmi, Vinamrata Singal, Richard Benes, et al. "STAT3 Modulation to Enhance Motor Neuron Differentiation in Human Neural Stem Cells." PLoS ONE 9, no. 6 (2014): e100405. http://dx.doi.org/10.1371/journal.pone.0100405.

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Seminary, Emily R., Stephanie Santarriaga, Lynn Wheeler, et al. "Motor Neuron Generation from iPSCs from Identical Twins Discordant for Amyotrophic Lateral Sclerosis." Cells 9, no. 3 (2020): 571. http://dx.doi.org/10.3390/cells9030571.

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Amyotrophic lateral sclerosis (ALS) is a complex neurodegenerative disorder characterized by the loss of the upper and lower motor neurons. Approximately 10% of cases are caused by specific mutations in known genes, with the remaining cases having no known genetic link. As such, sporadic cases have been more difficult to model experimentally. Here, we describe the generation and differentiation of ALS induced pluripotent stem cells reprogrammed from discordant identical twins. Whole genome sequencing revealed no relevant mutations in known ALS-causing genes that differ between the twins. As protein aggregation is found in all ALS patients and is thought to contribute to motor neuron death, we sought to characterize the aggregation phenotype of the sporadic ALS induced pluripotent stem cells (iPSCs). Motor neurons from both twins had high levels of insoluble proteins that commonly aggregate in ALS that did not robustly change in response to exogenous glutamate. In contrast, established genetic ALS iPSC lines demonstrated insolubility in a protein- and genotype-dependent manner. Moreover, whereas the genetic ALS lines failed to induce autophagy after glutamate stress, motor neurons from both twins and independent controls did activate this protective pathway. Together, these data indicate that our unique model of sporadic ALS may provide key insights into disease pathology and highlight potential differences between sporadic and familial ALS.

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Chang, Wei-Fang, Min Peng, Jing Hsu, et al. "Effects of Survival Motor Neuron Protein on Germ Cell Development in Mouse and Human." International Journal of Molecular Sciences 22, no. 2 (2021): 661. http://dx.doi.org/10.3390/ijms22020661.

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Survival motor neuron (SMN) is ubiquitously expressed in many cell types and its encoding gene, survival motor neuron 1 gene (SMN1), is highly conserved in various species. SMN is involved in the assembly of RNA spliceosomes, which are important for pre-mRNA splicing. A severe neurogenic disease, spinal muscular atrophy (SMA), is caused by the loss or mutation of SMN1 that specifically occurred in humans. We previously reported that SMN plays roles in stem cell biology in addition to its roles in neuron development. In this study, we investigated whether SMN can improve the propagation of spermatogonia stem cells (SSCs) and facilitate the spermatogenesis process. In in vitro culture, SSCs obtained from SMA model mice showed decreased growth rate accompanied by significantly reduced expression of spermatogonia marker promyelocytic leukemia zinc finger (PLZF) compared to those from heterozygous and wild-type littermates; whereas SMN overexpressed SSCs showed enhanced cell proliferation and improved potency. In vivo, the superior ability of homing and complete performance in differentiating progeny was shown in SMN overexpressed SSCs in host seminiferous tubule of transplant experiments compared to control groups. To gain insights into the roles of SMN in clinical infertility, we derived human induced pluripotent stem cells (hiPSCs) from azoospermia patients (AZ-hiPSCs) and from healthy control (ct-hiPSCs). Despite the otherwise comparable levels of hallmark iPCS markers, lower expression level of SMN1 was found in AZ-hiPSCs compared with control hiPSCs during in vitro primordial germ cell like cells (PGCLCs) differentiation. On the other hand, overexpressing hSMN1 in AZ-hiPSCs led to increased level of pluripotent markers such as OCT4 and KLF4 during PGCLC differentiation. Our work reveal novel roles of SMN in mammalian spermatogenesis and suggest new therapeutic targets for azoospermia treatment.

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Chang, Wei-Fang, Min Peng, Jing Hsu, et al. "Effects of Survival Motor Neuron Protein on Germ Cell Development in Mouse and Human." International Journal of Molecular Sciences 22, no. 2 (2021): 661. http://dx.doi.org/10.3390/ijms22020661.

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Survival motor neuron (SMN) is ubiquitously expressed in many cell types and its encoding gene, survival motor neuron 1 gene (SMN1), is highly conserved in various species. SMN is involved in the assembly of RNA spliceosomes, which are important for pre-mRNA splicing. A severe neurogenic disease, spinal muscular atrophy (SMA), is caused by the loss or mutation of SMN1 that specifically occurred in humans. We previously reported that SMN plays roles in stem cell biology in addition to its roles in neuron development. In this study, we investigated whether SMN can improve the propagation of spermatogonia stem cells (SSCs) and facilitate the spermatogenesis process. In in vitro culture, SSCs obtained from SMA model mice showed decreased growth rate accompanied by significantly reduced expression of spermatogonia marker promyelocytic leukemia zinc finger (PLZF) compared to those from heterozygous and wild-type littermates; whereas SMN overexpressed SSCs showed enhanced cell proliferation and improved potency. In vivo, the superior ability of homing and complete performance in differentiating progeny was shown in SMN overexpressed SSCs in host seminiferous tubule of transplant experiments compared to control groups. To gain insights into the roles of SMN in clinical infertility, we derived human induced pluripotent stem cells (hiPSCs) from azoospermia patients (AZ-hiPSCs) and from healthy control (ct-hiPSCs). Despite the otherwise comparable levels of hallmark iPCS markers, lower expression level of SMN1 was found in AZ-hiPSCs compared with control hiPSCs during in vitro primordial germ cell like cells (PGCLCs) differentiation. On the other hand, overexpressing hSMN1 in AZ-hiPSCs led to increased level of pluripotent markers such as OCT4 and KLF4 during PGCLC differentiation. Our work reveal novel roles of SMN in mammalian spermatogenesis and suggest new therapeutic targets for azoospermia treatment.

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Sun, Yubing, Koh Meng Aw Yong, Luis G. Villa-Diaz, et al. "Hippo/YAP-mediated rigidity-dependent motor neuron differentiation of human pluripotent stem cells." Nature Materials 13, no. 6 (2014): 599–604. http://dx.doi.org/10.1038/nmat3945.

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Grice, Stuart J., and Ji-Long Liu. "Survival Motor Neuron Protein Regulates Stem Cell Division, Proliferation, and Differentiation in Drosophila." PLoS Genetics 7, no. 4 (2011): e1002030. http://dx.doi.org/10.1371/journal.pgen.1002030.

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Catela, Catarina, Maggie M. Shin, David H. Lee, Jeh-Ping Liu та Jeremy S. Dasen. "Hox Proteins Coordinate Motor Neuron Differentiation and Connectivity Programs through Ret/Gfrα Genes". Cell Reports 14, № 8 (2016): 1901–15. http://dx.doi.org/10.1016/j.celrep.2016.01.067.

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Fornai, Francesco, Michela Ferrucci, Paola Lenzi, et al. "Plastic Changes in the Spinal Cord in Motor Neuron Disease." BioMed Research International 2014 (2014): 1–14. http://dx.doi.org/10.1155/2014/670756.

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In the present paper, we analyze the cell number within lamina X at the end stage of disease in a G93A mouse model of ALS; the effects induced by lithium; the stem-cell like phenotype of lamina X cells during ALS; the differentiation of these cells towards either a glial or neuronal phenotype. In summary we found that G93A mouse model of ALS produces an increase in lamina X cells which is further augmented by lithium administration. In the absence of lithium these nestin positive stem-like cells preferentially differentiate into glia (GFAP positive), while in the presence of lithium these cells differentiate towards a neuron-like phenotype (βIII-tubulin, NeuN, and calbindin-D28K positive). These effects of lithium are observed concomitantly with attenuation in disease progression and are reminiscent of neurogenetic effects induced by lithium in the subependymal ventricular zone of the hippocampus.

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Burtscher, Ingo, Marta Tarquis-Medina, Ciro Salinno, et al. "Generation of a Novel Nkx6-1 Venus Fusion Reporter Mouse Line." International Journal of Molecular Sciences 22, no. 7 (2021): 3434. http://dx.doi.org/10.3390/ijms22073434.

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Nkx6-1 is a member of the Nkx family of homeodomain transcription factors (TFs) that regulates motor neuron development, neuron specification and pancreatic endocrine and β-cell differentiation. To facilitate the isolation and tracking of Nkx6-1-expressing cells, we have generated a novel Nkx6-1 Venus fusion (Nkx6-1-VF) reporter allele. The Nkx6-1-VF knock-in reporter is regulated by endogenous cis-regulatory elements of Nkx6-1 and the fluorescent protein fusion does not interfere with the TF function, as homozygous mice are viable and fertile. The nuclear localization of Nkx6-1-VF protein reflects the endogenous Nkx6-1 protein distribution. During embryonic pancreas development, the reporter protein marks the pancreatic ductal progenitors and the endocrine lineage, but is absent in the exocrine compartment. As expected, the levels of Nkx6-1-VF reporter are upregulated upon β-cell differentiation during the major wave of endocrinogenesis. In the adult islets of Langerhans, the reporter protein is exclusively found in insulin-secreting β-cells. Importantly, the Venus reporter activities allow successful tracking of β-cells in live-cell imaging and their specific isolation by flow sorting. In summary, the generation of the Nkx6-1-VF reporter line reflects the expression pattern and dynamics of the endogenous protein and thus provides a unique tool to study the spatio-temporal expression pattern of this TF during organ development and enables isolation and tracking of Nkx6-1-expressing cells such as pancreatic β-cells, but also neurons and motor neurons in health and disease.

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Hudish, Laura I., Andrew Bubak, Taylor M. Triolo, et al. "Modeling Hypoxia-Induced Neuropathies Using a Fast and Scalable Human Motor Neuron Differentiation System." Stem Cell Reports 14, no. 6 (2020): 1033–43. http://dx.doi.org/10.1016/j.stemcr.2020.04.003.

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Nelson, Branden R., Karen Claes, Valerie Todd, Marta Chaverra, and Frances Lefcort. "NELL2 promotes motor and sensory neuron differentiation and stimulates mitogenesis in DRG in vivo." Developmental Biology 270, no. 2 (2004): 322–35. http://dx.doi.org/10.1016/j.ydbio.2004.03.004.

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Lu, David, Eric Y. T. Chen, Philip Lee, et al. "Accelerated Neuronal Differentiation Toward Motor Neuron Lineage from Human Embryonic Stem Cell Line (H9)." Tissue Engineering Part C: Methods 21, no. 3 (2015): 242–52. http://dx.doi.org/10.1089/ten.tec.2013.0725.

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Sagner, Andreas, Zachary B. Gaber, Julien Delile, et al. "Olig2 and Hes regulatory dynamics during motor neuron differentiation revealed by single cell transcriptomics." PLOS Biology 16, no. 2 (2018): e2003127. http://dx.doi.org/10.1371/journal.pbio.2003127.

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Abdullah, Rafal Hussamildeen, Shahlla Mahdi Salih, Nahi Yosef Yaseen, and Ahmed Majeed Al-Shammari. "Differentiation of Mouse Bone-Marrow Mesenchymal Stem Cells into Motor Neuron Cells in vitro." Journal of Al-Nahrain University-Science 19, no. 2 (2016): 111–16. http://dx.doi.org/10.22401/jnus.19.2.14.

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